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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pharmacological properties of 2 amino-4-[4-(2-hydroxyethyl)-piperazin-1-yl]-6-trifluoromethyl-s-triazine (TR-10) were investigated in mice and rats. Chlorpromazine served as a reference compound. Tr-10 expressed in general the pharmacological profiles as neuroleptic ascertained by anti-methamphetamine activity, supression of conditioned avoidance response, taming effects, decrease in exploratory behavior and cataleptogenic activity. Among these effects, anti-methamphetamine action was most potent. Different from chlorpromazine, TR-10 showed a similar pharmacological activity pattern in the intraperitoneal and oral routes of administration as depicted from ED50/LD50 values. Although the effects relevant to neuroleptics were less potent than chlorpromazine, such were seen with TR-10 at lower doses than those causing muscle relaxation. TR-10 significantly depressed the spontaneous motor activity but showed no anti-convulsant action in mice. Hypothermic action, potentiating effects of hypnotics and alpha-adrenergic blocking action, characteristic to chlorpromazine, were very weak for TR-10. TR-10 also showed low toxicity in mice (LD50 = 820 mg/kg p.o., 465 mg/kg i.p.) compared with that of chlorpromazine (LD50 = 370 mg/kg p.o., 228 mg/kg i.p.).
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PMID:Pharmacological studies on triazine derivatives V Sedative and neuroleptic actions of 2-amino-4-[4-(2-hydroxyethyl)-piperazin-1-yl]-6-trifluoromethyl-s-triazine (TR-10). 1 93

Sixteen cases of lactic acidosis are reported: 7 phenformin treated diabetes, 5 cardiovascular diseases (2 myocardial infractions, 2 pulmonary embolisms, 1 heart failure). In 2 patients no etiology was found. Concomittant renal failure or liver diseases were found in respectively 9 and 4 cases. Patients presented the usual criteria of lactic acidosis: clinical, polypnea, severe hypotension (9/16), peripheral symptoms of shock (12/16), hypothermia (9/16), abdominal pain (9/16): biologically, acidosis (pH = 6,99 +/- 0,01, HCO3- = 5,9 +/- 1,5 mmol), hyperlactatemia (14,1 +/- 3,6 mmol/l) with hig lactate/pyruvate ratio (105 +/- 73), and anion gap (24,3 +/- 4,2 mmol/l). Sodium bicarbonate infusion was performed in all cases (2,5 to 42 mmol/kg). Few cases required volhemic expansion or furosemid induced diuresis. One patient was treated with extrarenal dialysis. 13 patients were alkalinised with less than 185% of estimated deficit measured from alkalin reserve: 12 died. 3 patients received 185% more than this deficit, associated with furosemid (1,8 to 12,5 mg/kg): only one patient died ten days after by casual disease, with lactatemia of 3,2 mmol/l. In spite of the small number of patients, these findings suggest that an early and massive alkalinisation, with large doses of furosemid, can improve the severe lactic acidosis prognosis.
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PMID:[Lactic acidosis and intensive care. 16 cases (author's transl)]. 23 77

Acid-base terminology including the sue of SI units is reviewed. The historical reasons why nomograms have been particularly used in acid-base work are discussed. The theoretical basis of the Henderson-Hasselbalch equation is considered. It is emphasized that the solubility of CO2 in plasma and the apparent first dissociation constant of carbonic acid are not chemical constants when applied to media of uncertain and varying composition such as blood plasma. The use of the Henderson-Hasselbalch equation in making hypothermia corrections for PCO2 is discussed. The Astrup system for the in vitro determination of blood gases and derived parameters is described and the theoretical weakness of the base excess concept stressed. A more clinically-oriented approach to the assessment of acid-base problems is presented. Measurement of blood [H+] and PCO2 are considered to be primary data which should be recorded on a chart with in vivo CO2-titration lines (see below). Clinical information and results of other laboratory investigations such as plasma bicarbonate, PO2,P50 are then to be considered together with the primary data. In order to interpret this combined information it is essential to take into account the known ventilatory response to metabolic acidosis and alkalosis, and the renal response to respiratory acidosis and alkalosis. The use is recommended of a chart showing the whole-body CO2-titration points obtained when patients with different initial levels of non-respiratory [H+] are ventilated. A number of examples are given of the use of this [H+] and PCO2 in vivo chart in the interpretation of acid-base data. The aetiology, prognosis and treatment of metabolic alkalosis is briefly reviewed. Treatment with intravenous acid is recommended for established cases. Attention is drawn to the possibility of iatrogenic production of metabolic alkalosis. Caution is expressed over the use of intravenous alkali in all but the severest cases of metabolic acidosis. The role of 2,3-diphosphoglycerate on tissue oxygenation is stressed and use of intravenous sodium phosphate as an alternative to intravenous bicarbonate is mentioned.
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PMID:The physiological assessment of acid-base balance. 23 27

The synthesis and results of the pharmacologic assessment of new carbamic and carbonic acid esters with a stimulatory effect on the CNS are described. The structural analogues of carbamic acids are less toxic as compared to imipramine and to the respective derivatives of carbonic acid, and are also more active pharmacologically than some of the screening tests for antidepressant action. According to the test of antagonizing reserpine-induced hypothermia, the compounds coded 3a, 4a, 4c, 4d exert a stronger effect by comparison with that of imipramine.
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PMID:Synthesis and pharmacologic assessment of carbamic and carbonic acid esters with 1-aryl-3-dimethylamino-1-propanols. Part 3. 613 79

Alkaptonuria is a rare disease of phenylalanine, aromatic amino acids, and tyrosine metabolism. Because of a genetic deficiency of the enzyme homogentisic acid oxidase, an accumulation of homogentisic acid causes ochronotic pigment deposition. The most common clinical manifestations are arthropathy, urinary calculi and discoloration, cutaneous and cartilaginous pigmentation, and cardiac valvular disease. Arthropathy and aortic stenosis are the most debilitating manifestations of the disease. A case of alkaptonuric aortic stenosis is described. A 75-year-old woman with a history of alkaptonuria presented in the emergency department with complaints of progressive dyspnea. Upon examination, the patient was hypertensive, tachypneic, and tachycardic with premature ventricular contractions. She had pitting edema of the lower extremities and complaints of generalized weakness. Chest x-rays revealed congestive heart failure and pulmonary edema. Diuretics were administered, and a continuous nitroglycerin infusion was initiated in the emergency department. The patient was admitted for further evaluation. The patient's respiratory status continued to decline. She was intubated endotracheally 1 day after admission. Subsequent cardiac evaluation revealed an ejection fraction of 35%, severe aortic stenosis, mild coronary artery disease, ischemic cardiomyopathy, and anteroapical akinesis. A dobutamine infusion was instituted for persistent hypotension, and renal dose dopamine was initiated for oliguric renal failure. The patient underwent an emergency operation for an aortic valve replacement with a Dacron patch 10 days after admission. Cardiopulmonary bypass and mild hypothermia were used during the procedure. The patient's hemodynamic status remained tenuous throughout the procedure. Although the first attempt to wean off cardiopulmonary bypass failed, the second attempt was successful with the aid of an intra-aortic balloon pump, inotropic support, and atrioventricular pacing. These measures were maintained during transport to the surgical intensive care unit. In the intensive care unit, the patient did not have an audible blood pressure or a palpable pulse without the support of the intra-aortic balloon pump and atrioventricular pacing. Coarse atrial fibrillation was the underlying electrocardiogram rhythm in the absence of atrioventricular pacing. Sodium bicarbonate was given without improvement. After discussion with the family, all life support measures were discontinued. The patient died 10 minutes after her arrival in the intensive care unit. Alkaptonuria's pathogenesis is manifested as both local and systemic in nature. Collagen vascular diseases share a similar pattern of multisystem involvement. Despite the negative outcome for the patient described, valuable insight can be obtained by studying this case and noting the anesthetic considerations specific to collagen vascular diseases in general.
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PMID:Alkaptonuric aortic stenosis: a case report. 1048 88

The new CPR guidelines are based on a scientific consensus which was reached by 281 international experts. Chest compressions (100/min, 4-5 cm deep) should be performed in a ratio of 30:2 with ventilation (tidal volume 500 ml, Ti 1 s, FIO2 if possible 1.0). After a single defibrillation attempt (initially biphasic 150-200 J, monophasic 360 J, subsequently with the respective highest energy), chest compressions are initiated again immediately for 2 min. Endotracheal intubation is the gold standard; other airway devices may be employed as well depending on individual skills. Drug administration routes for adults and children: first choice IV, second choice intraosseous, third choice endobronchial [epinephrine dose 2-3x (adults) or 10x (pediatric patients) higher than IV]. Vasopressors: 1 mg epinephrine every 3-5 min IV. After the third unsuccessful defibrillation attempt amiodarone IV (300 mg); repetition (150 mg) possible. Sodium bicarbonate (1 ml/kg 8.4%) only in excessive hyperkalemia, metabolic acidosis, or intoxication with tricyclic antidepressants. Consider atropine (3 mg) and aminophylline (5 mg/kg). Thrombolysis during spontaneous circulation only in myocardial infarction or massive pulmonary embolism; during CPR only during massive pulmonary embolism. Cardiopulmonary bypass only after cardiac surgery, hypothermia or intoxication. Pediatrics: best improvement in outcome by preventing cardiocirculatory collapse. Alternate chest thumps and chest compression (infants), or abdominal compressions (>1-year-old) in foreign body airway obstruction. Initially five breaths, followed by chest compressions (100/min; approximately 1/3 of chest diameter): ventilation ratio 15:2. Treatment of potentially reversible causes (4 "Hs", "HITS": hypoxia, hypovolemia, hypo- and hyperkaliemia, hypothermia, cardiac tamponade, intoxication, thrombo-embolism, tension pneumothorax). Epinephrine 10 microg/kg IV or intraosseously, or 100 microg (endobronchially) every 3-5 min. Defibrillation (4 J/kg; monophasic oder biphasic) followed by 2 min CPR, then ECG and pulse check. Newborns: inflate the lungs with bag-valve mask ventilation. If heart rate<60/min chest compressions:ventilation ratio 3:1 (120 chest compressions/min). Postresuscitation phase: initiate mild hypothermia [32-34 degrees C for 12-24 h; slow rewarming (<0.5 degrees C/h)]. Prediction of CPR outcome is not possible at the scene; determining neurological outcome within 72 h after cardiac arrest with evoked potentials, biochemical tests and physical examination. Even during low suspicion for an acute coronary syndrome, record a prehospital 12-lead ECG. In parallel to pain therapy, aspirin (160-325 mg PO or IV) and in addition clopidogrel (300 mg PO). As antithrombin, heparin (60 IU/kg, max. 4000 IU) or enoxaparine. In ST-segment elevation myocardial infarction, define reperfusion strategy depending on duration of symptoms until PCI (prevent delay>90 min until PCI). Stroke is an emergency and needs to be treated in a stroke unit. A CT scan is the most important evaluation, MRT may replace a CT scan. After hemorrhage exclusion, thrombolysis within 3 h of symptom onset (0.9 mg/kg rt-PA IV; max 90 mg within 60 min, 10% of the entire dosage as initial bolus, no aspirin, no heparin within the first 24 h). In severe hemorrhagic shock, definite control of bleeding is the most important goal. For successful CPR of trauma patients, a minimal intravascular volume status and management of hypoxia are essential. Aggressive fluid resuscitation, hyperventilation, and excessive ventilation pressure may impair outcome in severe hemorrhagic shock. Despite bad prognosis, CPR in trauma patients may be successful in select cases. Any CPR training is better than nothing; simplification of contents and processes remains important.
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PMID:[The new 2005 resuscitation guidelines of the European Resuscitation Council: comments and supplements]. 1691 4